Studies during the past decade have provided a better understanding of the potential mechanisms responsible for the pathogenesis of preeclampsia. The initiating event in preeclampsia has been postulated to be reduced uteroplacental perfusion as a result of abnormal cytotrophoblast invasion of spiral arterioles. Placental ischemia/hypoxia is thought to lead to widespread activation/dysfunction of the maternal vascular endothelium which results in enhanced formation of endothelin, thromboxane, and superoxide, increased vascular sensitivity to angiotensin II, and decreased formation of vasodilators such as nitric oxide and prostacyclin. These endothelial abnormalities, in turn, cause hypertension by impairing renal function and increasing total peripheral resistance. While recent studies support a role for cytokines and other factors such as lipid peroxides and reactive oxygen intermediates as potential mediators of endothelial dysfunction, finding the link between placental ischemia/hypoxia and maternal endothelial and vascular abnormalities remains an important area of investigation. The quantitative importance of the various endothelial and humoral factors in mediating the vasoconstriction and elevation in arterial pressure during preeclampsia has also not been completely elucidated.